Thyroid hormone increases fibroblast growth factor receptor expression and disrupts cell mechanics in the developing organ of corti

Szarama, Katherine B.; Gavara, Núria; Petralia, Ronald S.; Chadwick, Richard S.; Kelley, Matthew W.

doi:10.1186/1471-213x-13-6

Cited by 17 publications

(16 citation statements)

References 102 publications

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“…This may suggest that VEGF inhibition occurred more strongly in cases with hypothyroidism [5]. Furthermore, there are several reports that the thyroid hormone is involved in the activation of FGFR [20][21][22][23], and lenvatinib has a strong inhibitory activity on FGFR [6]. Therefore, lenvatinib may be involved both in the onset of hypothyroidism and the long-term progression-free survival.…”

Section: Discussionmentioning

confidence: 98%

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

et al. 2019

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Lenvatinib has anti-tumor activity against advanced hepatocellular carcinoma (HCC). Hypothyroidism is also a frequent complication in patients treated with lenvatinib. However, studies on lenvatinib-induced thyroid toxicity and destructive thyroiditis are limited. Therefore, this study aimed to clarify the frequency and timing of thyroid abnormalities in lenvatinib for unresectable HCC. This retrospective study enrolled 50 patients with advanced HCC treated with lenvatinib. Patients were classified to have euthyroid, subclinical hypothyroidism, overt hypothyroidism, and thyrotoxicosis. The timing of thyroid dysfunction was assessed, and risk factors for incident hypothyroidism or thyrotoxicosis were evaluated using multivariate models. Subclinical hypothyroidism, overt hypothyroidism, and thyrotoxicosis occurred in 7 (14.0%), 26 (52.0%), and 5 (10.0%) patients, respectively. In the 33 patients with hypothyroidism, 27 (84.4%) developed the condition within 2 weeks of starting lenvatinib treatment. Of the 5 patients with thyrotoxicosis, 3 developed the condition within 8 weeks of starting lenvatinib administration. One patient developed thyrotoxicosis in only 1 week of the initiation of treatment. No correlation between the presence of antibodies and the incidence and severity of thyroid dysfunction due to the autoimmune mechanism was observed. The progression-free survival was significantly better in the hypothyroidism group. Lenvatinib treatment for unresectable HCC not only causes hypothyroidism, but also thyrotoxicosis. Moreover, these thyroid conditions develop within the early period of treatment at a higher prevalence. Patients with thyroid dysfunction had better prognosis. Based on these results, in patients administered with lenvatinib, there is need for careful assessment for the possibility of thyroid dysfunction from the onset of treatment.

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Section: Discussionmentioning

confidence: 98%

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

et al. 2019

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“…It is also possible to verify an insufficient formation and changes in microtubule stability with the rise of filamentous actin expression, which increases the stiffness and decreases the cell membrane mass. These changes directly affect the cochlear amplification process (28).…”

Section: Endocochlear Mechanisms Of Congenital Hypothyroidismmentioning

confidence: 99%

Mechanisms involved in hearing disorders of thyroid ontogeny: a literature review

Andrade

Machado

Fernandes

et al. 2017

Arch. Endocrinol. Metab.

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Endocochlear, retrocochlear and/or central origin hearing damage may be related to the absence of appropriate levels of thyroid hormone during morphogenesis and/or auditory system development. Hearing disorders related to the thyroid are not well studied, despite speculation on the pathophysiological mechanisms. The objective of this review was to characterize the main pathophysiological mechanisms of congenital hypothyroidism and to evaluate the relationship with central and peripheral hearing disorders. We conducted a literature review using the databases MedLine, LILACS, Cochrane Library, SciELO, Institute for Scientific Information (ISI), Embase, and Science Direct between July and September on 2016. We identified the studies that address hearing disorder mechanisms on the congenital hypothyroidism. Congenital hypothyroidism may have clinical and subclinical manifestations that affect the auditory system and may be a potential risk factor for hearing impairment. Hearing impairment can severely impact quality-of-life, which emphasizes the importance of monitoring and evaluating hearing during the clinical routine of these patients. Arch Endocrinol Metab. 2017;61(5):501-5

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“… 9 Alteration of thyroid hormones led to a decrease in acetylated tubulin immunofluorescence in supporting pillar and Deiters’ cells, and disrupted cell mechanics in the developing organ of Corti. 10 More recently, a report demonstrated that the reduction in acetylated α-tubulin labeling in the pillar cells in early postnatal stages was linked to mechanism of gjb2 -related hearing loss. 11 In the mammalian cochlea, the widespread expression of acetylated tubulin at different stages has been obtained, suggesting its expression in normal cochlea was related to the development.…”

Section: Introductionmentioning

confidence: 99%

Expression of acetylated tubulin in the postnatal developing mouse cochlea

Liu¹,

Wang²,

Yu³

et al. 2018

Eur J Histochem

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Microtubules are an essential component of the cytoskeleton of a eukaryotic cell. The post-translational tubulin modifications play an important role in regulating microtubule properties, acetylation tubulin is one of the major post-translational modifications of microtubules. Acetylation tubulin has also been shown to be expressed in the cochlea. However, the detailed expression profiles of acetylation tubulin protein during development have not yet been investigated in the postnatal mammalian cochlea. Here, we first examined the spatio-temporal expression of acetylated tubulin in the mouse cochlea during postnatal development. At postnatal day 1 (P1), acetylated tubulin was localized primarily to the auditory nerve inside the cochlea and their synaptic contacts with the inner and outer hair cells (IHCs and OHCs). In the organ of Corti, acetylated tubulin occurred first at the apex of pillar cells. At P5, acetylated tubulin first appeared in the phalangeal processes of Deiters’ cells. At P8, staining was maintained in the phalangeal processes of Deiters’ cells and neural elements. At P10, labeling in Deiters’ cells extended from the apices of OHCs to the basilar membrane, acetylated tubulin was expressed throughout the cytoplasm of inner and outer pillar cells. At P12, acetylated tubulin displayed prominent and homogeneous labeling along the full length of the pillar cells. Linear labeling was present mainly in the Deiters’ cell bodies underlying OHCs. Between P14 and P17, acetylated tubulin was strongly expressed in inner and outer pillar cells and Deiters’ cells in a similar pattern as observed in the adult, and labeling in these cells were arranged in bundles. In addition, acetylated tubulin was expressed in stria vascularis, root cell bodies, and a small number of fibrocytes of the spiral ligament until the adult. In the adult mouse cochlea, immunostaining continued to predominate in Deiters’ cells and pillar cells. In Deiters’ cells, immunolabeling formed cups securing OHCs basal portions, and continued presence of acetylated tubulin-labeled nerve terminals below IHCs was shown. Our results presented here underscored the essential role played by acetylated tubulin in postnatal cochlear development, auditory neurotransmission and cochlear mechanics.

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Thyroid hormone increases fibroblast growth factor receptor expression and disrupts cell mechanics in the developing organ of corti

Cited by 17 publications

References 102 publications

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

Lenvatinib-induced thyroid abnormalities in unresectable hepatocellular carcinoma

Mechanisms involved in hearing disorders of thyroid ontogeny: a literature review

Expression of acetylated tubulin in the postnatal developing mouse cochlea

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